BAX expression

This review is an attempt to elaborate molecular targets of luteolin and its role in modulating irregularities in cellular pathways to overcome severe outcomes during diseases including cancer, cardiovascular disorders, diabetes, obesity, inflammation, Alzheimer's disease, Parkinson's disease, hepatic disorders, renal disorders, brain injury, and asthma. As luteolin has enormous therapeutic benefits, it could be a potential candidate in future drug development strategies.

Bax and P21 protein levels were significantly upregulated following DNC treatment, whereas Bcl-2 and P53 protein levels were downregulated in DNC-treated breast cancer cells. In summary, dendrosomal nanocurcumin demonstrated potent anti-tumor effects against breast cancer cells, suggesting its potential as a therapeutic agent in breast cancer treatment.

The results indicate that GP might increase dopamine and serotonin levels in midbrain and promoted the survival of dopaminergic neurons in substantia nigra pars reticulata by regulating the expression of phosphorylation of MAPK family proteins and the expression of mitochondrial apoptosis-related proteins, and then ameliorate motor deficits in PD mice.

The co-delivery of CYC and SO via niosomes effectively targets apoptotic pathways in MDA-MB-231 breast cancer cells. The enhanced cytotoxicity and induction of apoptosis suggest that this drug delivery system may serve as an effective strategy for managing breast cancer.

It also restored the cardiac Sirt1/Nrf2/HO-1 signaling pathway. In conclusion, TAX showed significant cardioprotective effects on 5-FU-induced cardiac injury and might represent a promising adjuvant in preventing cardiac injury associated with oxidative stress and inflammation.

P4, N=90, Chongqing Health Center for Women and Children; Chongqing Health Center for Women and Children

Additionally, GADD45a and p21, involved in growth arrest and DNA damage, were significantly upregulated. In conclusion, citalopram's ability to induce apoptosis and alter cell cycle suggests its potential in breast cancer treatment.

MiR-490-3p upregulation inhibited cell proliferation and metastasis but promoted the cell apoptosis and cell-cycle arrest in osteosarcoma via the regulation of CDCA8/ATF3 by targeting NUSAP1. Thus, miR-490-3p might be a potential therapeutic target for the treatment of osteosarcoma.

As a results showed that NP and DX suppressed the proliferation of neuroblastoma cells and could do this through apoptotic pathways. NP can be used to suppress metastasis of SHSY-5Y cells as an inhibitor of the apoptosis pathway Bcl-2. It is thought that NP, which provides tumor suppression through an apoptotic mechanism, may be an alternative treatment agent in neurological cancers such as neuroblastoma.

Overall results revealed that HPME demonstrates a notable antioxidant capacity in human thyroid cancer. It exerts an influence on crucial biological processes associated with cancer, indicating its potential to hinder the proliferation of human thyroid cancer cells by enhancing apoptosis through the upregulation of gene and protein expression, particularly involving caspases.

IL-17A upregulates PD-L1 expression via the IL-17A receptor/phosphorylation-small mothers against decapentaplegic 2 signaling pathway in HCC cells. Blocking IL-17A enhances the therapeutic efficacy of PD-L1 antibodies in HCC in vivo.

Our findings demonstrate the therapeutic potential of FAELNs in UC management, highlighting their scalability for mass production and encouraging prospects for clinical transformation.

In addition, gilteritinib or GSK-J4 monotherapy increases reactive oxygen species (ROS) production, and the combination has a synergistic effect, accelerating leukemic cell death. Our study provides proof that the combined therapy of gilteritinib and GSK-J4 has a synergistic antileukemic effect on FLT3-ITD+ AML.

OsME exhibited antiproliferation activity on A549 cells and induced apoptosis at low doses.

Importantly, all of these changes induced by quinoa saponins were dose dependent. Overall, these findings give a scientific basis for the anticancer mechanism of quinoa saponins.

Taken together, this study suggests that PSTK could protect TEC viability from cisplatin-induced injury, possibly by inhibiting mitochondrial apoptosis. The study is significant for developing therapeutic strategies that could manipulate PSTK to delay AKI progression.

Transfection with miR-548m reduced FOXO3 mRNA and protein levels, while anti-miR-548m increased them. These findings suggest that GNC protects against H2O2-induced ovarian damage by modulating the miR-548m/FOXO3 axis, triggering autophagy and apoptosis.

Our results suggest that CW and its bioactive constituent CW1 enhance the antitumor activity of DTX by reducing P-gp expression and promoting phosphoinositide 3-kinase/Akt-mediated apoptosis in vitro and in vivo. Our results firstly confirm that CW1, as a natural bioactive substance, holds promise as an adjuvant drug for treating high-load metastatic and castration-resistant PCa.

Furthermore, the expression of proteins in the related signaling pathways TLR4, MyD88, and NF-κB was decreased. Resveratrol has been shown to reduce the expression of intestinal apoptotic proteins, enhance the expression of intestinal tight junction proteins, and inhibit the inflammatory response mediated by the TLR4/MyD88/NF-κB signaling pathway, thereby alleviating LPS-induced septic intestinal injury.

In addition, molecular docking analysis revealed that compound 13 could occupy the active site of p38α-MAPK well and interact to the surrounding amino acids by salt bridge and conjugation. These results suggested that compound 13 had the potential to serve as an antitumor lead agent, probably exert antitumor effect through mitochondrial pathway and p38α MAPK pathway.

Among the tested compounds, naphthyl- thiazoles demonstrated higher antiproliferative activity and B3 was identified as the most potent compound with IC50 values in the range of 2.03-3.6 µM against SH-SY5Y neuroblastoma, HT-29 colorectal adenocarcinoma, and fibroblast cells (ten folds more potent than 5-FU and irinotecan). Further investigation revealed that B3 strongly inhibits tubulin polymerization with an IC50 of 0.79 µM, outperforming the reference drug colchicine (IC50 = 1.46 µM)...In conclusion, our findings indicated that B3 in the thiazole congeners is a promising drug candidate for cancer treatment with a well-defined mechanism of action. Moreover, D4 and its congeners containing oxadiazole core are much safer anti-seizures which have potential for preclinical considerations as novel anticonvulsants.

"Zhibian" (BL54)-toward- "Shuidao" (ST28) acupuncture may ameliorate mouse reproductive function by inhibiting mitochondrial apoptosis pathway, alleviating testicular tissue damage in the asthenospermia mice induced by cyclophosphamide.

Curcumol may mediate the programmed death of AML cells by inhibiting the PI3K/AKT signaling pathway, affecting the expression of Bcl-2 family proteins, and promoting the activation of core members of Caspase family, so as to play an anti-leukemia role.

Our data demonstrated that solanine inhibits the proliferation and induces apoptosis of melanoma A375 and A2058 cells. The findings indicate that these effects may be associated with the mitochondrial apoptotic pathway.

The study's outcomes demonstrated that the introduction of Clostridium novyi-NT spores triggered apoptosis in cervical cancer cells (derived from the TC-1 cell line) via the mitochondrial pathway, subsequently resulting in tumor regression in a mouse model.

The findings of this study indicate that exosomal lncRNA H19 could be a diagnostic marker for Breast Cancer and these Breast cancer exosomes can induce malignant phenotype in fibroblasts and turn them into CAFs. Botox-A could be toxic for both normal fibroblasts and CAFs, inducing apoptosis and suppressing cell proliferation among them.

This study indicated that the potential mechanism of WJD in the prevention and treatment of CRC had the characteristics of the multi-target, multi-path, and multi-system mechanisms, which were mainly related to the regulation of chemokines and the promotion of apoptosis.

Luteolin induces apoptosis and autophagy to inhibit proliferation of A549 cells by increasing ROS production, inhibiting the AKT/mTOR pathway and down-regulating HO-1 protein expression.

PHPS1 can enhance PD-L1 serine phosphorylation by regulating SHP-2/AMPK activity to promote apoptosis of oral squamous cell carcinoma cells under hypoxic conditions.

The produced scFv antibody showed to be functional in a simultaneous blockade of EGFR and HER2, suggesting its potential as a promising candidate for targeted therapy against various EGFR overexpressing tumors.

Treatment with PD98059, SP600125, SB203580, or Bay 11-7082 reversed the effects of TNFRSF12A overexpression on cell proliferation, apoptosis, and proinflammatory cytokine expression. In conclusion, the effects of TNFRSF12A on proliferation, apoptosis, and proinflammatory cytokine expression in THCA cells were regulated by the MAPK and NF-κB pathways.

A gastric ulcer model was established using ethanol (ETH), and the experimental groups received either omeprazole (OMEP, 20 mg/kg) or SA at doses of 20 mg/kg and 40 mg/kg via oral gavage for 14 days...By targeting oxidative stress and inflammatory pathways, SA could complement or serve as an alternative to current treatment strategies. Future research should focus on exploring SA's molecular mechanisms, dose optimization, and long-term efficacy in clinical settings, paving the way for its integration into therapeutic regimens for gastric mucosal injuries.

Thereafter, flow cytometric apoptosis and protein expression of pro- and anti-apoptotic markers Bax, BCL-2, PI3K, and STAT1 proteins assays were performed employing the most active compound on the respective most responsive cell line and compounds demonstrated effectiveness in inducing apoptosis in the treated cell lines. Finally, in silico studies encompassing molecular docking and molecular dynamics studies were also conducted to predict the interaction mechanisms and stability of the active compounds within the active site of their biological target TS.

This study shows that overexpression of GDF15 reduces OGD/R-induced HT22 cell damage, and ER stress-mediated ferroptosis is included in the regulatory mechanisms. This provides a theoretical basis for GDF15 as a new target for the treatment of cerebral ischemia-reperfusion injury.

The pH-responsive drug delivery system has not only an excellent encapsulation rate but also a high drug loading capacity, and the doxorubicin loaded on it can be released centrally at the tumor microenvironment site and causes an increase of reactive oxygen species in the mitochondria and trigger oxidative stress, which leads to high expression of Bax apoptotic proteins, ultimately activating the mitochondrial pathway-mediated apoptotic process in glioma cells. Overall, this drug delivery system has great potential for application in precision targeted therapy and visual tracer imaging of gliomas.

Moreover, tropisetron successfully reinstated mitochondrial activity and diminished D-galactose-induced aberrant nitric oxide generation. The research concludes that tropisetron may provide protection against cardiac aging by activating multiple mechanisms associated with the SIRT1 pathway.

Our results advocate for the potential of metformin as a viable therapeutic option for preserving ovarian function in cyclophosphamide-treated adolescent girls, given its favorable side effect profile and ability to improve cyclophosphamide-induced ovarian damage.

In addition, ALG-12 inhibited the transcription of ataxia-telangiectasia mutated-and Rad3-related gene(ATR), tumor protein p53 gene(Tp53), Bcl-2 binding component 3 gene(BBC3), and Bcl-2 associated X protein gene(Bax) in the p53 signaling pathway, decreased the protein expression levels of p53, Bax, and cleaved caspase-3, and increased the protein expression levels of B-cell lymphoma/leukemia 2(Bcl-2) and caspase-3. The results suggested that ALG-12 had a protective effect on DDP-induced renal tubular epithelial cell injury, and the mechanism may be related to the inhibition of p53-mediated apoptosis, which provided a basis for further development of ALG-12.

PI3K inhibitor LY294002 intervention could reduce the promoting effect of AU on ribosome biogenesis. The above results suggest that AU can improve the injury of nucleus pulposus cells and ECM degradation, and its mechanism of action is related to its activation of the PI3K/mTOR pathway to promote ribosome biogenesis.

Activation of the p38 MAPK signaling pathway by anisomycin reduced the therapeutic effects of KAE. The study concluded that KAE could improve the proliferation activity of degenerated NPCs, reduce inflammation levels, and slow the progression of IDD in rats, and the mechanism was likely related to the regulation of the p38 MAPK signaling pathway.

R. roxburghii polysaccharides may inhibit the proliferation of DU145 cells and induce its apoptosis by inhibiting the PI3K/Akt/mTOR pathway and clearing intracellular ROS.

The positive control group received intraperitoneal injections of 5-fluorouracil(5-FU) at 20 mg·kg~(-1) every other day...Their mechanisms are related to TNF-α-mediated extrinsic apoptosis pathways and the induction of pyroptosis. The sensitivity of their action targets varies between American and Shandong ginsengs.